ArticleFrontiers in pharmacology2023
L-carnitine attenuated hyperuricemia-associated left ventricular remodeling through ameliorating cardiomyocytic lipid deposition.
Article in Frontiers in pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Oral L-carnitine supplementation lowers serum uric acid and is associated with renal and intestinal urate-handling responses in hyperuricemic mice.Frontiers in nutrition · 2026Article
- Comprehensive review of the expanding roles of the carnitine pool in metabolic physiology: beyond fatty acid oxidation.Journal of translational medicine · 2025Review
- Uric acid-induced cardiomyocytic polyamines' insufficience: a potential mechanism mediates cardiomyocytic injury.Frontiers in endocrinology · 2025Article
- A combination of red and processed meat intake and polygenic risk score influences the incidence of hyperuricemia in middle-aged Korean adults.Nutrition research and practice · 2024Article
- The Role of Hyperuricemia in Cardiac Diseases: Evidence, Controversies, and Therapeutic Strategies.Biomolecules · 2024Review
- The Dual Role of Uric Acid: Pathological Implications Across Chronic Diseases and Current Approaches to Hyperuricemia Management.Discoveries (Craiova, Romania)Review
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperuricemia (HUA) is associated with left ventricular remodeling (LVR) and thereby causes the initiation and development of a large number of cardiovascular diseases. LVR is typically accompanied by cardiomyocyte energy metabolic disorder. The energy supply of cardiomyocytes is provided by glucose and fatty acid (FA) metabolism. Currently, the effect of HUA on cardiomyocytic FA metabolism is unclear. In this study, we demonstrate that UA-induced cardiomyocyte injury is associated with cytoplasmic lipid deposition, which can be ameliorated by the FA metabolism-promoting drug L-carnitine (LC). UA suppresses carnitine palmitoyl transferase 1B (CPT1B), thereby inhibiting FA transport into the mitochondrial inner matrix for elimination. LC intervention can ameliorate HUA-associated left ventricular anterior wall thickening in mice. This study showed that FA transport dysfunction plays is a critical mechanism in both cardiomyocytic injury and HUA-associated LVR and promoting cytoplasmic FA transportation through pharmacological treatment by LC is a valid strategy to attenuate HUA-associated LVR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.